Journal
CHEMICO-BIOLOGICAL INTERACTIONS
Volume 283, Issue -, Pages 75-83Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2018.02.002
Keywords
Astrocytic senescent; Ginsenoside F1; p38MAPK; NF-kappa B; SASP; Glioblastoma
Funding
- Intelligent Synthetic Biology Center of the Global Frontier Project - Ministry of Education, Science and Technology, Republic of Korea
Ask authors/readers for more resources
Senescence is one of the hallmarks of aging and identified as a potential therapeutic target in the treatment of aging and aging-related diseases. Senescent cells accumulate with age in a variety of human tissues where they develop a complex senescence-associated secretory phenotype (SASP). SASP in brain could contribute to age-related inflammation and chronic neurodegenerative diseases. We confirmed that senescent astrocytes express a characteristic of SASP in vitro by human cytokine antibody array. Ginsenoside F1 suppresses the SASP from astrocytes induced by D-galactose via suppressing p38MAPK-dependent NF-kappa B activity. A specific inhibitor of p38MAPK, SB203580 significantly decreased the secretion of IL-6 and IL-8, the major components of SASPs. Additionally, treatment of senescent astrocytes with NF-kappa B inhibitor, BAY 11-7092, also suppressed the secretion of IL-6 and IL-8, suggesting NF-kappa B was required for SASP. Importantly, conditioned media from senescent astrocytes promoted the migration of glioblastoma cells, such as U373-MG, U251-MG and U87-MG assessed by scratch wound healing. This migration was significantly decreased by F1 treatment in senescent astrocytes. Interestingly, IL-8, the main mediator regulating glioblastoma cell invasion, was suppressed in both transcriptional and protein level. Herein, we propose ginsenoside F1 as a potential therapeutic strategy for reducing the deleterious contribution of senescent astrocytes in aged brain and related diseases.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available